The ability of species to adapt to changing and challenging conditions is remarkable and due to a wide variety of molecular mechanisms. Many of these mechanisms fall into the broad category of epigenetics of which we are still learning the details.
One of the best known epigenetic mechanisms is DNA methylation in which a small molecule (a methyl group) is added to the DNA macromolecule at particular locations. Like a barcode or marker, the methyl group indicates, for instance, which genes in the DNA are to be turned on. This DNA methylation is accomplished via the action of a protein machine that adds the methyl group at precisely the right location in the DNA strand.
The methylation occurs at certain target sites along the DNA sequence where specific short DNA sequences appear. These sequences are found by protein machines as they move along the DNA. The protein machines search for these sequences and add a methyl group to the appropriate DNA base.
The protein machine binds to the DNA, twists the helix so the DNA base rotates into a precisely shaped pocket in the protein, and the protein then facilitates the transfer of the methyl group from a short donor molecule to the DNA base.
In bacterial studies it has been found that the short donor molecule does more, however, than just supply a methyl group. It also helps to control the protein. First, the short donor molecule binds to the pocket of the protein so the methyl group is ready for transfer. But the donor molecule also binds to another site on the protein. This binding serves to alter the structure of the protein, enhancing its function. So the protein is designed to do its job when it is charged with a donor molecule.
But not all of the DNA target sequences are methylated. This complex DNA methylation function doesn’t occur if the target sequence is protected by another protein that binds to the sequence. This protein binds to some of these DNA target sequences but not all. The result is a particular DNA methylation pattern which influences which genes are expressed.
Mark the marker
Furthermore, the methyl group marker can, itself, be modified. That is, the mark can be marked, thus adding another layer of information to the epigenetic mechanism. For instance, the methyl group can be hydroxylated. And of course a different molecular machine is required for the task, and the information of when and where to go to work is needed.
All of this makes for a complex DNA methylation pattern which is superimposed on the DNA macromolecule. In fact, this encoding of epigenetic information varies substantially across different regions of the DNA and it varies between the two alleles of a given gene and this allele-specific methylation can be tissue-specific.
DNA methylation is also transmitted across generations, but in the embryonic stages of development can be erased by yet another protein machine.
In addition to the DNA macromolecule, methyl groups are also used to tag the histone proteins about which the DNA is wrapped. The histones have a hub, around which the DNA wraps, and a tail that sticks out on which chemical markers are attached. As with DNA, these markers are signals for the protein machinery. And like DNA, these tags are removed as well. Such modifications and removal of these chemical tags means that these codes are dynamic, and there are protein inspectors that double-check these complex encodings.
These subtle codes are also context dependent. In one type of cell a histone modification may turn off a gene whereas in another type of cell the same histone modification may turn on the gene.
In addition to methylation, histones can also vary by tiny differences in their amino acid sequence. This histone sequence variation serves as yet another type of tag used for gene regulation.
Furthermore, histone variants are not merely static sign posts that influence gene expression. These variants are moved, by other proteins, between different locations in the genome, resulting in migration patterns that occur in the embryonic development phases.
Did epigenetics evolve?
Evolutionists do not think twice about the question of whether the epigenetic world evolved. Of course it did. Evolution is a fact, and so all of biology is its handiwork. This despite the “hint at an unimagined complexity of the genome” as one science writer admitted.
With evolution we must be believe that levels of complexity we could never have dreamed of, and which contradict evolution’s predictions, arose from random mutations (no, natural selection doesn’t change that fact, the mutations are still random). And as those complex machines and mechanisms arose, we must either believe there would be no use for them, or just luckily there would be some intermediate use for them that they happened to fulfill, while waiting for a later time for their epigenetic functions to be realized.
In fact, beyond sheer speculation, there is no explanation for how the epigenetic world evolved. The conviction that it did evolve is not a scientific conclusion—it comes from the belief that evolution is a fact.
Of course none of this means that the epigenetic world absolutely could not have evolved. But there certainly is no justification for taking up positions at the other end of the spectrum. There is no scientific justification for proclaiming that evolution, including the evolution of the epigenetic world, is an undeniable fact, as evolutionists insist.
It is unfortunate that we stake out such hard-edged, dogmatic positions that can be defended only by shouting down and blackballing dissent. In spite of the science, evolution must be true and all who disagree must be rejected.
Evolutionists are not the first, and undoubtedly won’t be the last, to engage in religious narrow-mindedness and parochial intolerance, in defiance of the facts. Religion drives science, and it matters.